This project extends the examination of risk factors in cataractogenesis based on nutrient imbalances in tryptophan, vitamin E, and selenium. We determined that cataracts, which occur in rats from dams maintained on defined amino acid based diets with deficiencies in tryptophan and vitamin E, develop by a different mechanism from those which occur when rats, after weaning, are maintained on diets deficient in tryptophan. Vitamin E prevents cataract formation only in the congenital model. In attempts to describe developmental events which are susceptible to nutrient stress, we have determined that dietary excess in selenium provides added stress which leads to increased incidence of cataracts. Extremely predictable cataract formation is observed in neonates 72 h following injection with a single does of selenite, and is preceeded by decreases in lens glutathione and NADPH. Properties of this experimental system will be applied to specific objectives: 1) determination of how selenium effects the rapid and sustained supression of glutathione and initially alters NADPH turnover in the lens; 2) investigation of the mechanism linking the selenium- glutathione pertubation to cataract formation. 3) relating this information to what we understand about the low-tryptophan, low-vitamin E congenital cataract. 4) Evaluating the cataractogenic potential of chronic dietary selenium overload singly or in combination with other dietary imbalances known to be injurious to the lens. Our overall objective is to describe the sequence of events which results in cataract formation in both of these experimental models, so that we may understand as completely as possible the parameters which are required to maintain lens transparency. In the long term we hope to recognize which of these parameters is suceptible to nutritional manipulation. Such studies are requisite to our understanding of the impact of nutrition on the serious problem of senile catarat in the human population.